The heart is the center of a person's circulatory system. It includes an electro-mechanical system performing two major pumping functions. The left side of the heart, including the left atrium and left ventricle, draws oxygenated blood from the lungs and pumps it to various organs of the body to provide the organs with oxygen for their metabolic needs. This pumped blood flow is called the cardiac output. The right side of the heart, including the right atrium and right ventricle, draws deoxygenated blood from the organs and pumps it into the lungs where the blood gets oxygenated. The pumping functions are accomplished by contractions of the myocardium (heart muscles). In a normal heart, the sinoatrial node, the heart's natural pacemaker, generates electrical impulses, known as action potentials, that propagate through an electrical conduction system to various regions of the heart to excite myocardial tissues in these regions. Coordinated delays in the propagations of the action potentials in a normal electrical conduction system cause the various regions of the heart to contract in synchrony such that the pumping functions are performed efficiently.
Heart failure is a condition in which the myocardial muscle is weakened and its contractility is reduced, causing diminished cardiac output. A heart failure patient usually suffers from both a damaged electrical conduction system and a deteriorated myocardium. In response to the reduced cardiac output, the body attempts to adapt in a number of ways that lead to various symptoms as the heart failure condition progresses. A primary compensatory mechanism in heart failure includes increased sympathetic tone and an activated rennin-angiotensin system. This mechanism adversely reduces renal blood flow if the increased sympathetic tone and rennin-angiotensin activity persist. The body retains salt and water as a result of reduced renal blood flow. The salt and water are then accumulated in the lung and/or in peripheral tissues. Edema is caused by the increase of hydraulic pressure (reduction of oncotic pressure) in the circulation. The water retention may also lead to acute pulmonary edema, if the pulmonary capillary pressure reaches a certain level. In pulmonary edema, fluid leaks into the air sacs of the lung, causing the patient to gasp for breath. This condition can be fatal if not treated immediately. Another symptom of a patient with heart failure is fatigue on exertion. Once diagnosed with chronic heart failure, the patients is typically managed by interventions such as diet restriction and pharmacologic and/or device therapies. Such interventions keep the patient in a clinically stable state unless punctuated by episodes of acute heart failure decompensation. Acute heart failure decompensation is characterized by volume overload and shortness of breath, and requires immediate treatment in a hospital or an outpatient clinical setting.
Volume overload is the abnormally high blood volume resulting from fluid retention in the body including the circulatory system. A majority of hospitalization of heart failure patients is related to volume overload. Drug therapy has been applied to treat volume overload, thereby stopping or slowing the decompensation process. For example, diuretics are administrated orally (e.g., for decompensated heart failure) and intravenously (e.g., for acute decompensated heart failure) to restore fluid balance in the body. Because acute decompensated heart failure progresses rapidly after onset, a fast response upon early indications is needed.